| First Author | de S?? KSG | Year | 2026 |
| Journal | Cell | Volume | 189 |
| Issue | 11 | Pages | 3214-3235.e37 |
| PubMed ID | 42208499 | Mgi Jnum | J:387456 |
| Mgi Id | MGI:8349262 | Doi | 10.1016/j.cell.2026.04.042 |
| Citation | de Sa KSG, et al. (2026) A causal link between autoantibodies and neurological symptoms in long COVID. Cell 189(11):3214-3235.e37 |
| abstractText | Acute SARS-CoV-2 infection triggers the de novo production of diverse, functional autoantibodies (AABs) that remain elevated in long COVID (LC), but their pathogenic role remains unclear. Using tissue-based immunofluorescence, ELISA, human protein array, and mass spectrometry assays, we identified a broad range of AAB targets among individuals with LC. Individuals with neurocognitive symptoms showed increased AABs against central nervous system (CNS) and peripheral nervous system proteins. Purified immunoglobulin G (IgG) reacted with human locus coeruleus, thalamus, adrenal gland, and thyroid and cross-reacted with mouse sciatic nerve and meninges. CNS-reactive AABs correlated with several neurological symptoms. MED20-targeting IgG from patients with LC showed enhanced antibody-dependent phagocytosis. Passive transfer of IgG from individuals with LC into mice induced fatigue-like behavior, loss of balance/coordination, thermal hyperalgesia, small fiber nerve damage, and increased pain-related neuronal activity, recapitulating patients' symptoms. These findings suggest that targeting AABs might offer therapeutic benefits for this LC subgroup. |
